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PCI FOCUSED UPDATE

2007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention

American College of Cardiology/American Heart Association Task Force on Practice Guidelines 2007 Writing Group to Review New Evidence and Update the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention, Writing on Behalf of the 2005 Writing Committee, Spencer B. King, III, MD, MACC, FAHA, FSCAI, Co-Chair^_*,, Sidney C. Smith, Jr, MD, FACC, FAHA, Co-Chair^_*,, John W. Hirshfeld, Jr, MD, FACC, FAHA, FSCAI, Alice K. Jacobs, MD, FACC, FAHA, FSCAI, Douglass A. Morrison, MD, PhD, FACC, FSCAI, David O. Williams, MD, FACC, FAHA, FSCAI

^_* Chair of 2005 Writing Committee
Recused from voting on Section 7: Antiplatelet Therapy
Society for Cardiovascular Angiography and Interventions Representative
Recused from voting on Section 8: Bare-Metal and Drug-Eluting Stents

	2005 Writing Committee Members

Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

Ted E. Feldman, MD, FACC, FSCAI

John W. Hirshfeld, JR, MD, FACC, FAHA,FSCAI

Alice K. Jacobs, MD, FACC, FAHA, FSCAI

Morton J. Kern, MD, FACC, FAHA, FSCAI

Spencer B. King III, MD, MACC, FSCAI

Douglass A. Morrison, MD, PhD, FACC, FSCAI

William W. O’Neill, MD, FACC, FSCAI

Hartzell V. Schaff, MD, FACC, FAHA

Patrick L. Whitlow, MD, FACC, FAHA

David O. Williams, MD, FACC, FAHA,FSCAI

	Task Force Members

Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

 
Sidney C. Smith, Jr, MD, FACC, FAHA, Chair

Alice K. Jacobs, MD, FACC, FAHA, Vice-Chair

Cynthia D. Adams, MSN, PhD, FAHA^||

Jeffrey L. Anderson, MD, FACC, FAHA^||

Christopher E. Buller, MD, FACC

Mark A. Creager, MD, FACC, FAHA

Steven M. Ettinger, MD, FACC

Jonathan L. Halperin, MD, FACC, FAHA^||

Sharon A. Hunt, MD, FACC, FAHA^||

Harlan M. Krumholz, MD, FACC, FAHA

Frederick G. Kushner, MD, FACC, FAHA

Bruce W. Lytle, MD, FACC, FAHA

Rick Nishimura, MD, FACC, FAHA

Richard L. Page, MD, FACC, FAHA

Barbara Riegel, DNSc, RN, FAHA^||

Lynn G. Tarkington, RN

Clyde W. Yancy, MD, FACC

	Table of Contents

Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

 

Preamble......173

1 Introduction......175

1.1 Evidence Review......175

1.2 Organization of Committee and Relationships With Industry......175

1.3 Review and Approval......175

2 Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction......176

2.1 Electrocardiogram......179

2.1.1 Comparison of Early Invasive and Initial Conservative Strategies for UA/NSTEMI......181

2.1.2 Selection for Coronary Angiography......184

2.1.3 Chronic Kidney Disease......185

3 Facilitated PCI......186

4 Rescue PCI......187

5 PCI After Fibrinolysis or for Patients Not Undergoing Primary Reperfusion......190

6 Ancillary Therapy for Patients Undergoing PCI for STEMI......191

7 Antiplatelet Therapy......192

8 Bare-Metal and Drug-Eluting Stents......195

8.1 Selection of a Bare-Metal or Drug-Eluting Stent......195

9 Secondary Prevention......197

References......202

Appendix 1......206

Appendix 2......207

	Preamble

Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

 
A primary challenge in the development of clinical practice guidelines is keeping pace with the stream of new data upon which recommendations are based. In an effort to respond more quickly to new evidence, the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines has created a new "focused update" process to revise the existing guideline recommendations that are affected by evolving data or opinion. Before the initiation of this focused approach, periodic updates and revisions of existing guidelines required up to 3 years to complete. Now, however, new evidence will be reviewed in an ongoing fashion to more efficiently respond to important science and treatment trends that could have a major impact on patient outcomes and quality of care. Evidence will be reviewed at least twice a year, and updates will be initiated on an as needed basis as quickly as possible while maintaining the rigorous methodology that the ACC and AHA have developed during their more than 20 years of partnership.

These updated guideline recommendations reflect a consensus of expert opinion following a thorough review primarily of late-breaking clinical trials identified through a broad-based vetting process as important to the relevant patient population and of other new data deemed to have an impact on patient care (see Section 1.1 for details regarding this focused update). It is important to note that this focused update is not intended to represent an update based on a full literature review from the date of the previous guideline publication. Specific criteria/considerations for inclusion of new data include:

• Publication in a peer-reviewed journal

• Large, randomized, placebo-controlled trial(s)

• Nonrandomized data deemed important on the basis of results that impact current safety and efficacy assumptions

• Strengths/weakness of research methodology and findings

• Likelihood of additional studies influencing current findings

• Impact on current performance measure(s) and/or likelihood of the need to develop new performance measure(s)

• Requests and requirements for review and update from the practice community, key stakeholders, regulatory agencies, and other sources free of relationships with industry or other potential bias

• Number of previous trials showing consistent results

• Need for consistency with other new guidelines or guideline revisions

In analyzing the data and developing updated recommendations and supporting text, the focused update writing group used evidence-based methodologies developed by the ACC/AHA Task Force on Practice Guidelines, which are described elsewhere (1,2).

The schema for class of recommendation and level of evidence is summarized in Table 1, which also illustrates how the grading system provides estimates of the size of the treatment effect and the certainty of the treatment effect. Note that a recommendation with Level of Evidence B or C does not imply that the recommendation is weak. Many important clinical questions addressed in guidelines do not lend themselves to clinical trials. Although randomized trials may not be available, there may be a very clear clinical consensus that a particular test or therapy is useful and effective. Both the class of recommendation and level of evidence listed in the focused updates are based on consideration of the evidence reviewed in previous iterations of the guidelines as well as the focused update. Of note, the implications of older studies that have informed recommendations but have not been repeated in contemporary settings are carefully considered.

View this table: [in this window] [in a new window]   Table 1 Applying Classification of Recommendations and Level of Evidence

The ACC/AHA practice guidelines are intended to assist health care providers in clinical decision making by describing a range of generally acceptable approaches for the diagnosis, management, and prevention of specific diseases or conditions. The guidelines attempt to define practices that meet the needs of most patients in most circumstances. The ultimate judgment regarding care of a particular patient must be made by the health care provider and patient in light of all the circumstances presented by that patient. Thus, there are circumstances in which deviations from these guidelines may be appropriate. Clinical decision making should consider the quality and availability of expertise in the area where care is provided. These guidelines may be used as the basis for regulatory or payer decisions, but the ultimate goal is quality of care and serving the patient’s best interests.

Prescribed courses of treatment in accordance with these recommendations are only effective if they are followed by the patient. Because lack of patient adherence may adversely affect treatment outcomes, health care providers should make every effort to engage the patient in active participation with prescribed treatment.

The ACC/AHA Task Force on Practice Guidelines makes every effort to avoid any actual, potential, or perceived conflict of interest arising from industry relationships or personal interests of a writing committee member. All writing committee members and peer reviewers were required to provide disclosure statements of all such relationships pertaining to the trials and other evidence under consideration (see Appendixes 1 and 2). Final recommendations were balloted to all writing committee members. Writing committee members with significant (greater than $10 000) relevant relationships with industry (RWI) were required to recuse themselves from voting on that recommendation. Writing committee members who did not participate are not listed as authors of this focused update.

The recommendations in this focused update will be considered current until they are superseded by another focused update or the full-text guidelines are revised. This focused update is published in the January 15, 2008, issue of the Journal of the American College of Cardiology and the January 15, 2008, issue of Circulation and e-published in Catheterization and Cardiovascular Interventions as an update to the full-text guidelines and is also posted on the ACC (www.acc.org), AHA (www.americanheart.org), and Society for Angiography and Interventions (SCAI) (www.scai.org) Web sites. Copies of the focused update are available from all organizations.

Sidney C. Smith, Jr., MD, FACC, FAHA Chair, ACC/AHA Task Force on Practice Guidelines Alice K. Jacobs, MD, FACC, FAHA Vice-Chair, ACC/AHA Task Force on Practice Guidelines

	1. Introduction

Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

 
1.1 Evidence Review.   Selected late-breaking clinical trials presented at the 2005 and 2006 annual scientific meetings of the ACC, AHA, and European Society of Cardiology, as well as selected other data, were reviewed by the standing guideline writing committee along with the parent Task Force and other experts to identify those trials and other key data that might impact guideline recommendations. On the basis of the criteria/considerations noted above, recent trial data and other clinical information were considered important enough to prompt a focused update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention (3–13).

To provide clinicians with a comprehensive set of data, whenever possible, the exact event rates in various treatment arms of clinical trials are presented to permit calculation of the absolute risk difference (ARD) and number needed to treat (NNT) or harm (NNH); the relative treatment effects are described either as odds ratio (OR), relative risk (RR), or hazard ratio (HR), depending on the format in the original publication.

Consult the full-text version or executive summary of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention for policy on clinical areas not covered by the focused update (13a). Individual recommendations updated in this focused update will be incorporated into future revisions and/or updates of the full-text guidelines.

1.2 Organization of Committee and Relationships With Industry.   For this focused update, all members of the 2005 PCI writing committee were invited to participate; those who agreed (referred to as the 2007 focused update writing group) were required to disclose all RWI relevant to the data under consideration (2). Focused update writing group members who had no significant relevant RWI wrote the first draft of the focused update; the draft was then reviewed and revised by the full writing group. Each recommendation required a confidential vote by the writing group members before external review of the document. Any writing committee member with a significant (greater than $10 000) RWI relevant to the recommendation was recused from voting on that recommendation.

1.3 Review and Approval.   This document was reviewed by 2 outside reviewers nominated by each cosponsoring organization (ACC, AHA, and SCAI) and 24 individual content reviewers. All reviewer RWI information was collected and distributed to the writing committee and is published in this document (see Appendix 2 for details).

	2. Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction

Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

 
This 2007 PCI Focused Update section regarding patients with unstable angina (UA)/non–ST-elevation myocardial infarction (NSTEMI) is based on recommendations from the ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non–ST-Elevation Myocardial Infarction (14), which emphasize the importance of assessing risk of cardiovascular events as a guide to therapeutic decision making and the need for interventional therapy (see Table 2).

A number of risk-assessment tools have been developed to assist in assessing risk of death and ischemic events in patients with UA/NSTEMI, thereby providing a basis for therapeutic decision making. It should be recognized that the predictive ability of these commonly used risk assessment scores for risk of nonfatal coronary heart disease (CHD) is only moderate.

The Thrombolysis in Myocardial Infarction (TIMI) risk score (15) is a simple tool composed of 7 (1-point) risk indicators rated on presentation (Table 4). The composite end points (all-cause mortality, new or recurrent myocardial infarction [MI], or severe recurrent ischemia prompting urgent revascularization within 14 days) increase as the TIMI risk score increases. The TIMI risk score has been validated internally within the TIMI IIB trial and 2 separate cohorts of patients from the ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and Non–Q-Wave Myocardial Infarction) trial (16). The model remained a significant predictor of events and appeared relatively insensitive to missing information, such as knowledge of previously documented coronary stenosis of 50% or greater. The model’s predictive ability remained intact, with a cutoff of 65 years of age. The TIMI risk score was recently studied in an unselected emergency department population with chest pain syndrome; its performance was similar to that in the acute coronary syndrome (ACS) population from which it was derived and validated (17). The TIMI risk calculator is available at www.timi.org. The TIMI risk index, a modification of the TIMI risk score that uses the variables age, systolic blood pressure, and heart rate, has not only been shown to predict short-term mortality in ST-elevation myocardial infarction (STEMI) but also has been useful in prediction of 30-day and 1-year mortality rates across the spectrum of patients with ACS, including UA/NSTEMI (18).

The GRACE (Global Registry of Acute Coronary Events) study risk model, which predicts in-hospital mortality (and death or MI), can be useful to clinicians to guide treatment type and intensity (20,21). The GRACE risk tool was developed on the basis of 11 389 patients in GRACE and validated in subsequent GRACE and GUSTO (Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries) IIb cohorts and predicts in-hospital death in patients with STEMI, NSTEMI, or UA (C statistic=0.83). The 8 variables used in the GRACE risk model are older age (OR 1.7 per 10 years), Killip class (OR 2.0 per class), systolic blood pressure (OR 1.4 per 20 mm Hg decrease), ST-segment deviation (OR 2.4), cardiac arrest during presentation (OR 4.3), serum creatinine level (OR 1.2 per 1 mg per dL increase), positive initial cardiac markers (OR 1.6), and heart rate (OR 1.3 per 30-bpm increase). The sum of scores is applied to a reference nonogram to determine the corresponding all-cause mortality from hospital discharge to 6 months. The GRACE clinical application tool can be downloaded to a handheld PDA (personal digital assistant) to be used at the bedside and is available at www.outcomes-umassmed.org/grace (Figure 1) (21). An analysis comparing the 3 risk scores (TIMI, GRACE, and PURSUIT) concluded that all 3 demonstrated good predictive accuracy for death and MI at 1 year, thus identifying patients who might be likely to benefit from aggressive therapy, including early myocardial revascularization (22).

View larger version (35K): [in this window] [in a new window] [Download PPT slide]   Figure 1 GRACE Prediction Score Card and Nomogram for All-Cause Mortality From Discharge to 6 Months Reprinted with permission from (20). Copyright © 2004 American Medical Association.

The recommendations in the ACC/AHA 2007 UA/NSTEMI Guidelines (14) recognize recent data from the ACUITY (Acute Catheterization and Urgent Intervention Triage strategY) trial, which showed that in patients with ACS who were undergoing invasive treatment, bivalirudin alone was associated with rates of ischemia similar to those treated with glycoprotein (GP) IIb/IIIa inhibitors plus heparin and significantly less bleeding (25).

The ACC/AHA 2007 UA/NSTEMI Guidelines cite a progressively greater benefit from newer, more aggressive therapies such as low-molecular-weight heparin (LMWH) (16,26), platelet GP IIb/IIIa inhibition (27), and an invasive strategy (28) with increasing risk score.

2.1 Electrocardiogram.   The ECG lies at the center of the decision pathway for the evaluation and management of patients with acute ischemic discomfort (Table 5). The diagnosis of MI is confirmed with serial cardiac biomarkers in more than 90% of patients who present with ST-segment elevation greater than or equal to 1 mm (0.1 mV) in at least 2 contiguous leads, and such patients should be considered candidates for acute reperfusion therapy. Patients who present with ST-segment depression are initially considered to have either UA or NSTEMI; the distinction between the 2 diagnoses is ultimately based on the detection of markers of myocardial necrosis in the blood (29–31).

In addition to the presence or absence of ST-segment deviation or T-wave inversion patterns noted earlier, there is evidence that the magnitude of the ECG abnormality provides important prognostic information. Thus, Lloyd-Jones et al. (41) reported that the diagnosis of acute non–Q-wave MI was 3 to 4 times more likely in patients with ischemic discomfort who had at least 3 ECG leads that showed ST-segment depression and maximal ST depression of greater than or equal to 0.2 mV. Investigators from the TIMI III Registry (42) reported that the 1-year incidence of death or new MI in patients with at least 0.5 mm (0.05 mV) of ST-segment deviation was 16.3% compared with 6.8% for patients with isolated T-wave changes and 8.2% for patients with no ECG changes.

Cardiogenic shock can occur in the setting of both STEMI and NSTEMI, and there is high mortality and morbidity in each. The SHOCK (SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK) study (43) found that approximately 20% of all cardiogenic shock complicating MI was associated with NSTEMI. The GUSTO-II (44) and PURSUIT (45) trials found that cardiogenic shock occurs in up to 5% of patients with NSTEMI and that mortality rates are greater than 60%. Thus, hypotension and evidence of organ hypoperfusion can occur and constitute a medical emergency in NSTEMI.

2.1.1 Comparison of Early Invasive and Initial Conservative Strategies for UA/NSTEMI
Prior meta-analyses concluded that routine invasive therapy (the "invasive" or "early" strategy triages patients to undergo an invasive diagnostic evaluation without first getting a noninvasive stress test or without failing medical treatment [i.e., an initial conservative diagnostic strategy or sometimes now known as the "selective invasive strategy"] (14)) is better than an initial conservative or selectively invasive approach (the "initial conservative strategy" [also referred to as "selective invasive management"] calls for proceeding with an invasive evaluation only for those patients who fail medical therapy [refractory angina or angina at rest or with minimal activity despite rigorous medical therapy] or in whom objective evidence of ischemia [dynamic ECG changes, high-risk stress test] is identified (14)). Mehta et al. (47) concluded that the routine invasive strategy resulted in an 18% relative reduction in death or MI, including a significant reduction in MI alone. The routine invasive arm was associated with higher in-hospital mortality (1.8% versus 1.1%), but this disadvantage was more than compensated for by a significant reduction in mortality between discharge and the end of follow-up (3.8% versus 4.9%). In those analyses, the invasive strategy was associated with less angina and fewer rehospitalizations than the conservative pathway. Patients undergoing routine invasive treatment also had improved quality of life.

In contrast to these findings, other studies, most recently ICTUS (Invasive versus Conservative Treatment in Unstable coronary Syndromes), have favorably highlighted a strategy of selective invasive therapy (48). In ICTUS, 1200 high-risk ACS patients without ST-segment elevation were randomized to receive routine invasive versus selective invasive management and followed up for 1 year with respect to the combined incidence of death, MI, and ischemic rehospitalization. All patients were treated with optimal medical therapy that included aspirin, clopidogrel, LMWH, and lipid-lowering therapy; abciximab was given to those undergoing revascularization. At the end of 1 year, there was no significant difference in the composite end point between groups. This study suggests that a selective invasive strategy could be reasonable for ACS patients. A possible explanation for the lack of benefit of the invasive approach in this trial (and other trials) (49) could be related to the relatively high rate of revascularization actually performed in patients treated in the selective invasive arm (47%), thereby reducing observed differences between treatment strategies (22), and to the lower event rate (lower-risk population) than in other studies. Results were unchanged during longer-term follow-up (50,51). Nevertheless, ICTUS required troponin positivity for entry. Thus, troponin alone might no longer be an adequate criterion for strategy selection, especially with increasingly sensitive troponin assays. The degree of troponin elevation and other high-risk clinical factors taken together should be considered in selecting a treatment strategy. The ICTUS trial was relatively underpowered for hard end points, and it used a controversial definition for post procedural MI (i.e., even minimal asymptomatic CK-MB elevation) (48,50,51).

Additionally, 1-year follow-up may be inadequate to fully realize the long-term impact and benefit of the routine invasive strategy. In the RITA-3 trial (Third Randomized Intervention Trial of Angina), 5-year but not 1-year event rates favored the early invasive arm (see Figure 2 and text below) (52). In ICTUS, however, results were maintained during a 3-year follow-up (53).

View larger version (18K): [in this window] [in a new window] [Download PPT slide]   Figure 2 Cumulative Risk of Death or Myocardial Infarction in RITA-3 Top: Cumulative risk of death or myocardial infarction in the RITA-3 trial of patients with non-ST acute coronary syndrome. Bottom: Cumulative risk of death in the RITA-3 trial of patients with non-ST acute coronary syndromes. Reprinted with permission from (52).

Nevertheless, a meta-analysis of contemporary randomized trials in NSTEMI, including ICTUS, currently support long-term mortality and morbidity benefits of an early invasive compared with an initial conservative strategy (54). Nonfatal MI at 2 years (7.6% vs. 9.1%, respectively; RR 0.83 [95% CI 0.72 to 0.96]; p = 0.012) and hospitalization (at 13 months; RR = 0.69 [95% CI 0.65 to 0.74]; p less than 0.0001) also were reduced by an early invasive strategy (Figure 3). A separate review of contemporary randomized trials in the stent era using the Cochrane Database arrived at similar conclusions (55). Details of selected contemporary trials of invasive versus conservative strategies may be found in the ACC/AHA 2007 UA/NSTEMI Guidelines (14).

View larger version (15K): [in this window] [in a new window] [Download PPT slide]   Figure 3 Relative Risk of Outcomes With Early Invasive Versus Conservative Therapy in UA/NSTEMI A: Relative risk of all-cause mortality for early invasive therapy compared with conservative therapy at a mean follow-up of 2 years. B: Relative risk of recurrent nonfatal myocardial infarction for early invasive therapy compared with conservative therapy at a mean follow-up of 2 years. C: Relative risk of recurrent unstable angina resulting in rehospitalization for early invasive therapy compared with conservative therapy at a mean follow-up of 13 months (54). CI indicates confidence interval; FRISC-II, FRagmin and fast Revascularization during InStability in Coronary artery disease; ICTUS, Invasive versus Conservative Treatment in Unstable coronary Syndromes; ISAR-COOL, Intracoronary Stenting with Antithrombotic Regimen COOLing-off; RITA-3, Third Randomized Intervention Trial of Angina; RR, relative risk; TIMI-18, Thrombolysis In Myocardial Infarction-18; TRUCS, Treatment of Refractory Unstable angina in geographically isolated areas without Cardiac Surgery; UA/NSTEMI, unstable angina/non–ST-elevation myocardial infarction; and VINO, Value of first day angiography/angioplasty In evolving Non-ST segment elevation myocardial infarction: Open multicenter randomized trial. Modified with permission from (54).

In the VINO trial (Value of first day angiography/ angioplasty In evolving Non-ST segment elevation myocardial infarction: Open multicenter randomized trial) (58), 131 patients with NSTEMI were randomized to cardiac catheterization on the day of admission versus conservative therapy. Despite the fact that 40% of the conservatively treated patients crossed over to revascularization by the 6-month follow-up, there was a significant reduction in death or reinfarction for patients assigned to early angiography and revascularization (6% versus 22%).

The ISAR-COOL (Intracoronary Stenting with Antithrombotic Regimen Cooling-off) trial (59) randomized 410 intermediate- to high-risk patients to very early angiography and revascularization versus a delayed invasive strategy. All patients were treated with intensive medical therapy that included aspirin, heparin, clopidogrel (600-mg loading dose), and the intravenous GP IIb/IIIa receptor inhibitor tirofiban. In the very early arm, patients underwent cardiac catheterization at a mean time of 2.4 hours versus 86 hours in the delayed invasive arm. The very early invasive strategy was associated with significantly better outcome at 30 days, as measured by reduction in death and large MI (5.9% versus 11.6%). More importantly, the benefit seen was attributable to a reduction in events before cardiac catheterization, which raises the possibility that there is a hazard associated with a "cooling-down" period.

2.1.2 Selection for Coronary Angiography
In contrast to the noninvasive tests, coronary angiography provides detailed structural information to allow assessment of prognosis and provide direction for appropriate management. When combined with left ventricular (LV) angiography, it also allows an assessment of global and regional LV function. Indications for coronary angiography are interwoven with indications for possible therapeutic plans, such as PCI or CABG.

Coronary angiography is usually indicated in patients with UA/NSTEMI who either have recurrent symptoms or ischemia despite adequate medical therapy or are at high risk as categorized by clinical findings (HF, serious ventricular arrhythmias) or noninvasive test findings (significant LV dysfunction: ejection fraction less than 0.35, large anterior or multiple perfusion defects) (Tables 6, 7, and 8). Patients with UA/NSTEMI who have had previous PCI or CABG also should generally be considered for early coronary angiography unless prior coronary angiography data indicate that further revascularization is not likely to be possible. The placement of an intra-aortic balloon pump (IABP) may allow coronary angiography and revascularization in those with hemodynamic instability. Patients with suspected Prinzmetal’s variant angina also are candidates for coronary angiography.

2.1.3 Chronic Kidney Disease
The following recommendations have been added to the PCI Focused Update in accordance with new recommendations appearing in the 2007 UA/NSTEMI Guidelines (14) (Table 9). Supporting text from that guidelines statement is presented in the following paragraphs.

Particularly in the setting of ACS, bleeding complications are higher in this patient subgroup because of platelet dysfunction and dosing errors; benefits of fibrinolytic therapy, antiplatelet agents, and anticoagulants can be negated or outweighed by bleeding complications; and renin-angiotensin-aldosterone inhibitors can impose a greater risk because of the complications of hyperkalemia and worsening renal function in the patient with CKD. Angiography carries an increased risk of contrast-induced nephropathy; the usual benefits of PCI can be lessened or abolished; and PCI in patients with CKD is associated with a higher rate of early and late complications of bleeding, restenosis, and death (68). Thus, identification of CKD is important in that it represents an ACS subgroup with a far more adverse prognosis but for whom interventions have less certain benefit.

Coronary arteriography is a frequent component of the care of ACS patients. As such, contrast-induced nephropathy can constitute a serious complication of diagnostic and interventional procedures. In patients with CKD or CKD and diabetes, isosmolar contrast material lessens the rise in creatinine and is associated with lower rates of contrast-induced nephropathy than low-osmolar contrast media. This has been documented in a randomized clinical trial (RECOVER [Renal Toxicity Evaluation and Comparison Between Visipaque (Iodixanol) and Hexabrix (Ioxaglate) in Patients With Renal Insufficiency Undergoing Coronary Angiography]) comparing iodixanol with ioxaglate (71) and in a meta-analysis of 2727 patients from 16 randomized clinical trials (72).

Identification of patients with CKD as recommended in the AHA Science Advisory on Detection of CKD in patients with or at increased risk of CVD should guide the use of isosmolar contrast agents (63). The advisory, which was developed in collaboration with the National Kidney Foundation, recommends that all patients with CVD be screened for evidence of kidney disease by estimating glomerular filtration rate, testing for microalbuminuria, and measuring the albumin-to-creatinine ratio. A glomerular filtration rate of less than 60 ml per min per 1.73 square meters of body surface should be regarded as abnormal. Furthermore, the albumin-to-creatinine ratio should be used to screen for the presence of kidney damage in adult patients with CVD, with values greater than 30 mg of albumin per 1 g of creatinine considered abnormal.

A diagnosis of renal dysfunction is critical to proper medical therapy for UA/NSTEMI. Many cardiovascular drugs used in patients with UA/NSTEMI are renally cleared; their doses should be adjusted for estimated creatinine clearance [see also Section 3 of the 2007 UA/NSTEMI Guidelines (14)]. In a large community-based registry study, 42% of patients with UA/NSTEMI received excessive initial dosing of at least 1 antiplatelet or antithrombin agent (unfractionated heparin [UFH], LMWH, or GP IIb/IIIa inhibitor) (73). Renal insufficiency was an independent predictor of excessive dosing. Dosing errors predicted an increased risk of major bleeding. Clinical studies and labeling that defines adjustments for several of these drugs have been based on the Cockcroft-Gault formula for estimating creatinine clearance, which is not identical to the Modification of Diet and Renal Disease (MDRD) formula. Use of the Cockcroft-Gault formula to generate dose adjustments is recommended. The impact of renal dysfunction on biomarkers of necrosis (i.e., troponin) is discussed in Section 2.2.8.2.1 of the 2007 UA/NSTEMI Guidelines (14).

To increase the meager evidence base and to optimize care for this growing high-risk population, the recognition of CKD patients with or at risk of CVD and the inclusion and reporting of renal disease in large CVD trials must be increased in the future.

3. Facilitated PCI.   Facilitated PCI refers to a strategy of planned immediate PCI after administration of an initial pharmacological regimen intended to improve coronary patency before the procedure. These regimens have included high-dose heparin, platelet GP IIb/IIIa inhibitors, full-dose or reduced-dose fibrinolytic therapy, and the combination of a GP IIb/IIIa inhibitor with a reduced-dose fibrinolytic agent (e.g., fibrinolytic dose typically reduced 50%). Facilitated PCI should be differentiated from primary PCI without fibrinolytic therapy, from primary PCI with a GP IIb/IIIa inhibitor started at the time of PCI, from early or delayed PCI after successful fibrinolytic therapy, and from rescue PCI after unsuccessful fibrinolytic therapy. Potential advantages of facilitated PCI include earlier time to reperfusion, smaller infarct size, improved patient stability, lower infarct artery thrombus burden, greater procedural success rates, higher TIMI flow rates, and improved survival rates. Potential risks include increased bleeding complications, especially in older patients; potential limitations include added cost.

Despite the potential advantages, clinical trials of facilitated PCI have not demonstrated any benefit in reducing infarct size or improving outcomes. The largest of these was the ASSENT-4 (Assessment of the Safety and Efficacy of a New Treatment Strategy with Percutaneous Coronary Intervention) PCI trial (5), in which 1667 patients were randomized to full-dose tenecteplase and PCI versus primary PCI. The trial was terminated prematurely because of a higher in-hospital mortality rate in the facilitated PCI group (6% vs. 3%, p = 0.01). The primary end point, a composite of death, shock, and congestive heart failure within 90 days, was significantly higher with facilitated PCI than with primary PCI (18.6% vs. 13.4%; p = 0.0045), and there was a trend toward higher 90-day mortality (6.7% vs. 4.9%; p = 0.14). Defenders of the facilitated PCI strategy point out that the absence of an infusion of heparin after bolus administration and of a loading dose of clopidogrel, plus prohibition of GP IIb/IIIa inhibitors except in bail-out situations, made adjunctive antithrombotic therapy suboptimal for the facilitated PCI group. Moreover, the median treatment delay between tenecteplase and PCI was only 104 minutes, and mortality rates with facilitated PCI were higher in PCI centers. Whether earlier (pre-hospital) administration of fibrinolytic therapy, better antithrombotic therapy, longer delays to PCI, or selective use of PCI as a rescue strategy would make the facilitated PCI strategy beneficial is unclear and requires further study. On the basis of these data, however, facilitated PCI offered no clinical benefit.

Keeley and coworkers performed a quantitative review of 17 trials that compared facilitated PCI and primary PCI (74) (Figure 4). Included were 9 trials with GP IIb/IIIa inhibitors alone (n = 1148), 6 trials with fibrinolytic therapy (including ASSENT-4 PCI) (n = 2953), and 2 trials with a fibrinolytic agent plus a GP IIb/IIIa inhibitor (n = 399). Facilitated PCI with fibrinolytic therapy had significantly higher rates of mortality, nonfatal reinfarction, urgent target vessel revascularization, total and hemorrhagic stroke, and major bleeding compared with primary PCI. There were no differences in efficacy or safety when facilitated PCI with a GP IIb/IIIa inhibitor was compared with primary PCI.

View larger version (29K): [in this window] [in a new window] [Download PPT slide]   Figure 4 Short-Term Death in Patients Treated With Facilitated Or Primary PCI Trials were classified by facilitated regimen. Diamonds and squares indicate odds ratios. Lines indicate 95% confidence intervals. Reprinted with permission from (74).

The 2005 PCI Guideline Update (13a) recommendations for rescue PCI were based on observational data and 2 small randomized clinical trials (n = 179) from the early 1990s (94,95). More recently, MERLIN (Middlesbrough Early Revascularization to Limit Infarction) (n = 307) and REACT (Rescue Angioplasty versus Conservative Treatment or Repeat Thrombolysis) (n = 427) and 3 meta-analyses have refocused attention on rescue PCI (96–100). This subject has been studied with fewer than 1000 patients enrolled in randomized trials.

In the period between trials studying rescue PCI, there was a transition between angiographic and electrocardiographic diagnosis to detect failed reperfusion. Importantly, in the earlier studies, rescue PCI was performed in infarct arteries with TIMI 0/1 flow, often after a protocol-mandated 90-minute angiogram. In MERLIN and REACT, however, patients were randomized if they had less than 50% ST-segment elevation resolution at 60 or 90 minutes, respectively. Many patients had patent infarct arteries at angiography; only 54% of patients in MERLIN and 74% of patients in REACT (which required less than TIMI grade 3 flow for PCI) actually underwent PCI. From a procedural standpoint, stents have replaced balloon angioplasty, antiplatelet therapy has improved with the addition of a thienopyridine agent and often a GP IIb/IIIa receptor antagonist, and procedural success rates are higher.

Despite these historical differences, recent data support the initial observation that rescue PCI decreases adverse clinical events compared with medical therapy. In the Wijeysundera meta-analysis (100) (Figure 5), there was a trend toward reduced mortality rates with rescue PCI from 10.4% to 7.3% (RR 0.69 [95% CI 0.46 to 1.05]; p = 0.09), reduced reinfarction rates from 10.7% to 6.1% (RR 0.58 [95% CI 0.35 to 0.97]; p = 0.04), and reduced HF rates from 17.8% to 12.7% (RR 0.73 [95% CI 0.54 to 1.00]; p = 0.05). These event rates suggest that high-risk patients were selected for enrollment, so these data do not define the role of rescue PCI in lower-risk patients. Also, the benefits of rescue PCI need to be balanced against the risk. There was an excess occurrence of stroke in 2 trials (10 events versus 2 events), but the majority were thromboembolic rather than hemorrhagic, and the sample size was small, so more data are required to define this risk. There was also an increase of 13% in absolute risk of bleeding, suggesting that adjustments in antithrombotic medication dosing are needed to improve safety. It should be noted that the majority of patients who underwent rescue PCI received streptokinase as fibrinolytic therapy.

View larger version (36K): [in this window] [in a new window] [Download PPT slide]   Figure 5 Efficacy End Points for Rescue PCI Versus Conservative Therapy CI indicates confidence interval; MERLIN, Middlesbrough Early Revascularization to Limit Infarction trial; NNT, number needed to treat; PCI, percutaneous coronary intervention; REACT, Rescue Angioplasty versus Conservative Treatment or Repeat Thrombolysis trial; RESCUE, Randomized Comparison of Rescue Angioplasty with Conservative Management of Patients with Early Failure of Thrombolysis for Acute Anterior Myocardial Infarction trial; RR, relative risk; and TAMI, Thrombolysis and Angioplasty in Myocardial Infarction study. Reprinted with permission from (100).

5. PCI After Fibrinolysis or for Patients Not Undergoing Primary Reperfusion.   The open artery hypothesis suggests that late patency of an infarct artery is associated with improved LV function, increased electrical stability, and provision of collateral vessels to other coronary beds for protection against future events (see Table 12). The OAT (Occluded Artery Trial) (12) tested the hypothesis that routine PCI for total occlusion 3 to 28 days after MI would reduce the composite of death, reinfarction, or Class IV heart failure. Stable patients (n = 2166) with an occluded infarct artery after MI (about 20% of whom received fibrinolytic therapy for the index event) were randomized to optimal medical therapy and PCI with stenting or optimal medical therapy alone. The qualifying period of 3 to 28 days was based on calendar days; thus, the minimal time from symptom onset to angiography was just over 24 hours. Inclusion criteria included total occlusion of the infarct-related artery with TIMI grade 0 or 1 antegrade flow and LV ejection fraction (LVEF) less than 50% or proximal occlusion of a major epicardial artery with a large risk region. Exclusion criteria included NYHA Class III or IV heart failure, serum creatinine greater than 2.5 mg per dL, left main or 3-vessel disease, clinical instability, or severe inducible ischemia on stress testing if the infarct zone was not akinetic or dyskinetic. The 4-year cumulative end point was 17.2% in the PCI group and 15.6% in the medical therapy group (HR 1.16 [95% CI 0.92 to 1.45] p = 0.2). Reinfarction rates tended to be higher in the PCI group, which may have attenuated any benefit in LV remodeling. There was no interaction between treatment effect and any subgroup variable.

6. Ancillary Therapy for Patients Undergoing PCI for STEMI.   The 2007 STEMI Guidelines Focused Update (106) includes a new section on the use of anticoagulant therapy for patients undergoing PCI to establish reperfusion for STEMI. The recommendations associated with PCI are summarized in Table 13.

Given the complexities of the characteristics of the individual agents and their actions on the coagulation cascade, clinicians are cautioned about extrapolating any of the observations with agents discussed in this update to other anticoagulant regimens. In particular, as noted by the Food and Drug Administration (FDA), the LMWHs are sufficiently distinct that they should be evaluated individually rather than considered as a class of interchangeable agents (110).

7. Antiplatelet Therapy.   The 2005 PCI Guideline Update (13a) recommended aspirin antiplatelet therapy of 325 mg, which was based primarily on results from the TAXUS IV and SIRIUS trials (111–128). Since that time, experience has been gained with doses of aspirin ranging from 75 mg to 325 mg (see Table 14 for further information and Table 15 for a list of the trials). No significant trials have been reported comparing lower-dose aspirin (75 mg to 100 mg) with higher-dose aspirin (162 mg to 325 mg) in subacute or late stent thrombosis with the incidence of bleeding as the initial course of therapy after placement of drug-eluting stents (DES). Two major trials (129,130) involving patients not undergoing placement of DES report an increase in risk of bleeding on higher-dose aspirin. No conclusive data are available regarding higher-dose aspirin and subacute stent thrombosis among patients who are considered aspirin resistant.

Likewise, clopidogrel 75 mg daily should be given for a minimum of 1 month after implantation of a BMS [minimum 2 weeks for patients at significant increased risk of bleeding (132)] and for 12 months after implantation of a SES or PES and ideally in all patients post PCI who are not at high risk of bleeding. Under urgent circumstances that prevent the use of clopidogrel for 1 year, the duration studied for FDA approvals was 3 months for an SES and 6 months for a PES. The optimal duration of clopidogrel therapy after 1 year has not been established and should depend on the judgment of the risk–benefit ratio for the individual patient. Predictors of late stent thrombosis have included stenting of small vessels, multiple lesions, long stents, overlapping stents, ostial or bifurcation lesions, prior brachytherapy, suboptimal stent result, low ejection fraction, advanced age, diabetes mellitus, renal failure, ACS, and premature discontinuation of antiplatelet agents (133,134). Patients should be counseled on the need for and risks of DAT before placement of intracoronary stents, especially a DES, and alternative therapies to pursue if they are unwilling or unable to comply with the recommended duration of DAT. To reduce the incidence of bleeding complications associated with DAT, lower-dose aspirin (75 mg to 162 mg daily) is reasonable for long-term therapy (135,136). Given the importance of a 1-year course of DAT, it is recommended that elective surgery be postponed for 1 year, and among those patients for whom surgery cannot be deferred, aspirin therapy should be considered during the perioperative period in high-risk patients with DES (133).

Several investigations have explored various loading doses of clopidogrel before or during PCI. Consistent findings are that compared with a 300-mg loading dose, doses of either 600 or 900 mg achieve greater degrees of platelet inhibition with less variability among patients (137). Fewer patients may demonstrate "resistance" or nonresponsiveness to clopidogrel following the 600-mg dose. There appears to be no significant additive value of the 900-mg dose over the 600-mg dose (137).

The 600-mg dose appears to achieve maximum inhibition more rapidly than the 300-mg dose (138). Superior clinical outcomes at 30 days, primarily reduction in evidence of MI, have been reported after the 600-mg dose given 2 hours before the procedure, although this salutary effect was not confirmed in 1 investigation (139). No excess hazard has been reported with the 600-mg compared with the 300-mg dose for patients treated with fibrinolytic therapy; however, loading doses greater than 300 mg have not been studied (140). Larger trials will more fully evaluate higher doses of clopidogrel on clinical events, as well as further evaluate safety (e.g., bleeding). The OASIS-7 trial is comparing 600-mg with 300-mg loading doses of clopidogrel and will provide further evidence about the optimal treatment strategy.

There is agreement that the loading dose should be administered before PCI. What is unclear is the precise time when the loading dose must be given to achieve a desirable therapeutic effect. Evidence from the CREDO (Clopidogrel for the Reduction of Events During Observation) trial suggests that with a 300-mg dose, 6 hours is the minimum time (131). With the 600-mg dose, 2 hours may be sufficient (141), although maximal platelet inhibition may not be achieved until 3 to 4 hours (142).

Long-term clopidogrel therapy alone may not achieve adequate inhibition for PCI. Patients on long-term therapy with clopidogrel experience significant additional incremental inhibition of platelet aggregation when given a loading dose (143). In patients treated with fibrinolytic therapy, however, loading doses of greater than 300 mg have not been studied (144).

8. Bare-Metal and Drug-Eluting Stents.   8.1 Selection of a Bare-Metal or Drug-Eluting Stent
Observational studies indicate that physicians routinely implant stents when performing coronary interventions. Two types of stents are available: BMS and DES. Drug-eluting stents have become increasingly popular as standard therapy. In 2005, a sampling of 140 US hospitals indicated that 94% of patients treated with a stent received at least 1 DES (145). More recently, however, because of concerns about stent thrombosis and the mandate that each DES-treated patient take prolonged DAT, the proportion of DES use has declined to 60% to 70%.

The results of the clinical trials that led to FDA approval of the DES provide support for its use in suitable patients. Extended follow-up of the initial investigated patient cohorts to 4 years confirms the sustained benefit of DES in decreasing the need for repeat revascularization but without differences in death or MI (146–148). Randomized clinical trials in selected clinical subsets such as BMS in-stent restenosis, total occlusions, diabetes mellitus, and small-diameter arteries have also demonstrated the value of DES and have prompted physicians to extend the application of DES beyond the narrow patient populations included in the initial approval trials (122,126,149–154). The duration of follow-up of these "off-label" studies and the small number of patients enrolled, however, limit the detection of subtle differences in important end points such as stent thrombosis, death, or MI.

It is important to recognize certain differences between the BMS and DES when selecting a stent for an individual patient or lesion. First, in general, a DES may be more difficult to implant than a BMS. The DES has a polymer coating that stiffens the stent and makes it less conformable. Accordingly, one reason for using a BMS is that it can be used in patients in whom a DES cannot be implanted successfully. Second, the DES is substantially more expensive than the BMS. When financial resources are limited, use of the DES may be rationed, with implantation only in those patients at greatest risk for restenosis.

A third but very important difference relates to the inhibition of endothelial coverage of the DES and the need for extended DAT (Table 16). After introduction of the BMS, it was associated with a disturbingly high incidence of stent thrombosis (141). Stent thrombosis often presented as MI or even death and usually occurred in the first 30 days after implantation. Changes in technique such as high inflation pressure and intravascular ultrasound (IVUS)-guided deployment and use of concomitant combined aspirin and thienopyridine therapy substantially reduced the incidence of stent thrombosis to a clinically acceptable level (155). Importantly, the requisite duration of DAT was only 4 weeks, and some advocated only 2 weeks. The importance of DAT in preventing stent thrombosis was further strengthened by the outcome of patients for whom DAT was discontinued prematurely because of the need for those patients to undergo surgical procedures. These patients experienced a disturbingly high incidence of stent thrombosis (156). The critical role of DAT in preventing stent thrombosis was also noted among patients with BMS who had received brachytherapy for in-stent restenosis. Presumably these patients were less likely to develop subsequent neointimal coverage of the endoluminal stent surface and were accordingly then more susceptible to stent thrombosis.

The tight relationship between DAT and stent thrombosis for patients treated with DES warrants emphasis and has implications for selecting the type of stent deployed at the time of PCI. For example, the clinician should not select a DES for a patient who does not have access to DAT for financial reasons or who is unlikely to be compliant in taking DAT. One study revealed that 14% of patients had stopped DAT 1 month after implantation of the DES (158). Also, implantation of a BMS may be more appropriate in a patient with a known increased risk of bleeding. In situations such as these, the consequences of developing restenosis are considered less untoward than those of stent thrombosis or significant bleeding.

Furthermore, prescribed premature discontinuation of DAT in patients treated with a DES should not be done casually. For example, routine dental procedures should not justify cessation of DAT even though it is anticipated DAT will be subsequently resumed (133). Consideration should be given to delay scheduling of elective procedures that normally warrant discontinuation of antiplatelet agents. The benefit of DES in reducing the need for target vessel revascularization (TVR) also should be taken into account. Some registries have shown 1-digit TVR rates with the BMS, and the absolute reduction in these events using the DES depends on patient and lesion characteristics.

There are also concerns related to the appropriate duration of DAT. More recently, the occurrence of late (up to 1 year) or very late (beyond 1 year) stent thrombosis among DES-treated patients has been described (159). One database analysis suggests that extended use of DAT may have value in preventing late stent thrombosis, whereas others disagree (160).

Outcomes of patients in the initial FDA-approval trials to 4 years provides reassurance that, at least for those types of patients, despite a small excess of stent thrombosis, there appears to be no increase in death or MI when comparing DES-treated groups with BMS-treated groups. As noted, protocol-recommended DAT in these patients was not more than 6 months, although extended DAT was not prohibited. (These results are observed despite a significant excess occurrence of stent thrombosis among patients who received a paclitaxel stent.) Some have postulated that the substantial additional revascularization procedures experienced by BMS patients were associated with a small but significant excess rate of death and MI that offset any deaths or MIs that may have occurred in the DES group related to stent thrombosis.

Less data are available regarding the outcomes of patients who receive a DES for an "off-label" indication. Such patients have characteristics of their coronary disease, for example, a lesion in an artery less than 2.5 mm in diameter, very long lesions, bifurcation lesions, or a clinical syndrome such as acute MI, that were excluded in the FDA-approval trials. Reports from large observational studies indicate that "off-label" patients may experience higher rates of repeat revascularization and death and MI at 1 year than DES patients with "on-label" features. Importantly, a similar relationship is observed for patients treated with a BMS. In addition, there appears to be a significant association between "off-label" use and stent thrombosis. Accordingly, the appropriate selection for DAT among "off-label" DES patients may be different than for "on-label" patients.

At this point in time, 12 months of DAT is recommended for all patients who receive a DES (120) (see Section 6.2.1) unless there is a high risk of bleeding. The benefits and indications for treatment with DAT beyond 1 year in patients with DES are the subject of ongoing studies. Low-dose aspirin should be continued indefinitely. For patients with clinical features associated with stent thrombosis, such as renal insufficiency, diabetes, or procedural characteristics such as multiple stents or treatment of a bifurcation lesion, extended DAT beyond 1 year may be reasonable. The risk of stent thrombosis needs to be balanced with other medical conditions and nonmedical factors that might affect the risk-benefit ratio of DAT versus other therapies. Finally, certain DES-treated patients have already discontinued DAT 1 year after stent implantation. No information yet supports restarting DAT in these patients.

9. Secondary Prevention.   Table 17 presents revised recommendations based on the 2006 AHA/ACC Secondary Prevention Guidelines for Patients with Coronary and Other Atherosclerotic Vascular Diseases (11). This table replaces Table 26 from the 2005 PCI Guideline Update (13a). Classes of recommendation and a corresponding level of evidence have been added for all recommendations. There is a new recommendation for annual influenza vaccination, and the section on antiplatelet agents/anticoagulants has been modified slightly to reflect the recent evidence on aspirin dosage in patients who have undergone PCI with stent placement. Other changes since publication of the 2006 ACC/AHA Secondary Prevention Guidelines include the addition of recommended daily physical activity and a Class IIa recommendation for lowered low-density lipoprotein cholesterol.

John C. Lewin, MD, Chief Executive Officer

Charlene May, Director, Clinical Policy and Documents

Lisa Bradfield, Associate Director, Practice Guidelines

Kristen N. Fobbs, MS, Senior Specialist, Practice Guidelines

Mark D. Stewart, MPH, Associate Director, Evidence-Based Medicine

Sue Keller, BSN, MPH, Senior Specialist, Evidence-Based Medicine

Erin A. Barrett, Senior Specialist, Clinical Policy and Documents

American Heart Association

M. Cass Wheeler, Chief Executive Officer

Rose Marie Robertson, MD, FACC, FAHA, Chief Science Officer

Judy Bezanson, DSN, CNS, RN, Science and Medicine Advisor

	Appendix

Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

 

	Footnotes

 
This document is a limited update to the 2005 guideline update and is based on a review of certain evidence, not a full literature review.

This document was approved by the American College of Cardiology Board of Trustees in October 2007, by the American Heart Association Science Advisory and Coordinating Committee in October 2007, and by the Society for Cardiovascular Angiography and Interventions Board of Trustees in November 2007.

The American College of Cardiology Foundation, American Heart Association, and Society for Cardiovascular Angiography and Interventions request that this document be cited as follows: King SB III, Smith SC Jr., Hirshfeld JW Jr., Jacobs AK, Morrison DA, Williams DO. 2007 focused update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines: (2007 Writing Group to Review New Evidence and Update the 2005 ACC/AHA/SCAI Guideline Update for Percutaneous Coronary Intervention). J Am Coll Cardiol 2008;51:172–209.

This article has been copublished in the January 15, 2008, issue of Circulation and e-published in Catheterization and Cardiovascular Interventions.

Copies: This document is available on the World Wide Web sites of the American College of Cardiology (www.acc.org), American Heart Association (www.americanheart.org), and Society for Cardiovascular Angiography and Interventions (www.scai.org). For copies of this document, please contact Elsevier Inc. Reprint Department, fax 212-633-3820, e-mail reprints{at}elsevier.com.

Permissions: Modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American College of Cardiology and the American Heart Association. Please contact the American Heart Association: Instructions for obtaining permission are located at http://www.americanheart.org/presenter.jhtml?identifier=4431. A link to the "Permission Request Form" appears on the right side of the page.

Society for Cardiovascular Angiography and Interventions Representative

^|| Former Task Force member during this writing effort

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Top 2005 Writing Committee Members Task Force Members Table of Contents Preamble 1. Introduction 2. Patients With Unstable... Appendix References

 
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